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Congenital anophthalmia and microphthalmia are rare developmental defects of the globe. They often arise in conjunction with other ocular defects such as coloboma and orbital cyst. They may also be part of more generalised syndromes, such as CHARGE syndrome. Anophthalmia, microphthalmia, and coloboma are likely to be caused by disturbances of the morphogenetic pathway that controls eye development, either as a result of primary genetic defect, or external gestational factors, including infection or drugs that can influence the smooth processes of morphogenesis. The ophthalmologist is often the primary carer for children with anophthalmia and microphthalmia, and as such can coordinate the multidisciplinary input needed to offer optimal care for these individuals, including vision and family support services. They are able to assess the vision and maximise the visual potential of the child and they can also ensure that the cosmetic and social impact of anophthalmia or microphthalmia is minimised by starting socket expansion or referring to a specialist oculoplastics and prosthetics unit. A coordinated approach with paediatrics is necessary to manage any associated conditions. Genetic diagnosis and investigations can greatly assist in providing a diagnosis and informed genetic counselling.

Congenital anophthalmia and microphthalmia are rare developmental defects of the globe. They often arise in conjunction with other ocular defects such as coloboma and orbital cyst. They may also be part of more generalised syndromes, such as CHARGE syndrome. Anophthalmia, microphthalmia, and coloboma are likely to be caused by disturbances of the morphogenetic pathway that controls eye development, either as a result of primary genetic defect, or external gestational factors, including infection or drugs that can influence the smooth processes of morphogenesis. The ophthalmologist is often the primary carer for children with anophthalmia and microphthalmia, and as such can coordinate the multidisciplinary input needed to offer optimal care for these individuals, including vision and family support services. They are able to assess the vision and maximise the visual potential of the child and they can also ensure that the cosmetic and social impact of anophthalmia or microphthalmia is minimised by starting socket expansion or referring to a specialist oculoplastics and prosthetics unit. A coordinated approach with paediatrics is necessary to manage any associated conditions. Genetic diagnosis and investigations can greatly assist in providing a diagnosis and informed genetic counselling.

Comparison of the herpes simplex virus type 1 (HSV-1) DNA sequence with that of other alpha, beta and gamma-herpesviruses, allied with molecular genetic studies have greatly increased understanding of the HSV genome and the functions encoded by individual virus genes and has facilitated the development of rational antiviral strategies. Here we review the coding content of the HSV-1 genome and identify: genes encoding structural components of the capsid, tegument or envelope; genes whose products are essential for growth in tissue culture; and genes that are conserved between members of the alpha, beta and gamma-herpesvirinae. The HSV lifecycle and the main regulation cascade is discussed and genes that present targets for antiviral intervention identified. The protein content of the infectious virion particle is reviewed and compared with that of two additional non-infectious HSV-related particles species (L-particles and pre-DNA replication particles (PREPs)). The potential of HSV-1 L particles and PREP particles as DNA-free HSV-1 vaccine candidates and the desirability of deleting specific gene products from live HSV vaccines is discussed.

To identify suitable host cells permissive for virus growth but resistant to the triterpenoid compound cicloxolone sodium (CCX), 18 cell lines were studied for tolerance to treatment for 48 h with increasing drug concentrations. IC50 values and replication indices of the IC50, at 300 μm CCX and in the absence of drug, were determined. Eight cell lines proved resistant, six sensitive and four intermediate in sensitivity to CCX. Four of the resistant cell lines were then selected as appropriate hosts for investigating the antiviral effect of CCX. Infectious yield dose–response experiments were carried out with viruses from eight different families comprising enveloped and non-enveloped DNA and RNA viruses. The RNA viruses included some with genomes that were segmented or non-segmented, positive-stranded, negative-stranded or double-stranded. No consistent relationship between sensitivity to CCX and any of these characteristics was found. Three classes of response were obtained: class 1 [VSV (Indiana), Influenza A, EHV-1 and BHV-1] showed a consistent, progressive CCX dose-dependent 100→100000-fold reduction in infectious virus yield; class 2 (Bunyamwera and Germiston, Polio-1, Reovirus-3 and Adenovirus-5) exhibited initial sensitivity (10–100-fold) but increasing the dose had minimal further effect on yield, with plateau values reached between 100 and 200 μm CCX; class 3 (SFV) appeared to be unaffected by CCX treatment. Plaque reduction assays revealed that HCMV and VZV are also highly sensitive to CCX inhibition.

At the recommended clinical dose for direct application to infected wounds tetrachloro decaoxide (TCDO) (1.0 × concentration TCDO) alone or in combination with haemoglobin proved to be cytotoxic for BHK and Flow 2002 cells, but at ≤0.1 TCDO/haem concentration BHK-21 cells tolerated treatment with the drug for 24 h retaining ≥80% cell viability. The in vitro cytotoxic effect is only partially reversible; but this could not explain the strong antiviral effect of TCDO/haem against herpes simplex virus type 1 (HSV-1) growing in BHK cells. The antiviral effect produces both a reduction in the number of virus particles assembled, and a lowering of their relative infectivity (i.e. reduced virus quality). The antiviral effect was active throughout the HSV-1 replication cycle. The quality of the viral DNA that was packaged into particles was unimpaired but unpackaged DNA was less infectious than controls. The reduction in particle numbers appeared to be due to both lowered protein synthesis and reduced virus particle assembly. TCDO/haem exhibits potent virucidal activity against HSV-1; HSV-2; Semliki Forest virus; Germiston virus; Reovirus type 3; Influenza virus type A; Feline leukaemia virus; Adenovirus type 5 and Polio virus type 1. Enveloped viruses, though varying over a wide sensitivity range were more sensitive than non-enveloped viruses. The magnitude of the virucidal effect against HSV-1 in suspension could be reduced by addition of BSA. The HSV-1 virucidal effect stems mainly from an effect of the drug on virion polypeptides. We propose that the effects of TCDO/haem result from the nonspecific chemical oxidation of susceptible chemical linkages both within and between individual proteins located intracellularly (antiviral and cytotoxic effects) or on the surface of virions (virucidal effect).

A comparative study of seven independently isolated defective leukaemia viruses has been carried out. Phenotypic analysis of the chicken bone marrow cells transformed in vitro allowed the separation of these seven viruses into three groups based on the differentiation phenotype of the transformed cell. Nucleic acid hybridization studies revealed that these seven viruses had acquired cellular sequences. Interestingly, these studies also showed that the viruses within the same biological grouping had acquired related sequences. This indicates that viruses that have acquired the same or similar cellular sequences have very similar oncogenic capabilities. Analysis of proteins expressed in cells transformed by these viruses demonstrated that the cellular sequences were usually inserted within the gene for the viral core proteins, gag. Therefore the cellular sequences are expressed as a gag-related fusion protein which has an amino-terminal region derived from the gag gene and a carboxy-terminal half derived from the cellular sequences. Two exceptions to this are discussed. The general conclusion from these studies is that defective leukaemia viruses transform cells by virtue of acquired host cellular sequences. The ability of these viruses to transform cells and the target cell specificity of the transformation depends on these cellular sequences.